TY - INPR A1 - Hou, Liping A1 - Bergen, Sarah E. A1 - Akula, Nirmala A1 - Song, Jie A1 - Hultman, Christina M. A1 - Landén, Mikael A1 - Adli, Mazda A1 - Alda, Martin A1 - Ardau, Raffaella A1 - Arias, Bárbara A1 - Aubry, Jean-Michel A1 - Backlund, Lena A1 - Badner, Judith A. A1 - Barrett, Thomas B. A1 - Bauer, Michael A1 - Baune, Bernhard T. A1 - Bellivier, Frank A1 - Benabarre Hernandez, Antonio A1 - Bengesser, Susanne A1 - Berrettini, Wade H. A1 - Bhattacharjee, Abesh Kumar A1 - Biernacka, Joanna A1 - Birner, Armin A1 - Bloss, Cinnamon S. A1 - Brichant-Petitjean, Clara A1 - Bui, Elise T. A1 - Byerley, William A1 - Cervantes, Pablo A1 - Chillotti, Caterina A1 - Cichon, Sven A1 - Colom, Francesc A1 - Coryell, William A1 - Craig, David W. A1 - Cruceanu, Cristiana A1 - Czerski, Piotr M. A1 - Davis, Tony A1 - Dayer, Alexandre A1 - Degenhardt, Franziska A1 - Del Zompo, Maria A1 - DePaulo, J. Raymond A1 - Edenberg, Howard J. A1 - Étain, Bruno A1 - Falkai, Peter A1 - Foroud, Tatiana A1 - Forstner, Andreas Josef A1 - Frisén, Louise A1 - Frye, Mark A. A1 - Fullerton, Janice M. A1 - Gard, Sébastien A1 - Garnham, Julie S. A1 - Gershon, Elliot S. A1 - Goes, Fernando S. A1 - Greenwood, Tiffany A. A1 - Grigoroiu-Serbanescu, Maria A1 - Hauser, Joanna A1 - Heilbronner, Urs A1 - Heilmann-Heimbach, Stefanie A1 - Herms, Stefan A1 - Hipolito, Maria A1 - Hitturlingappa, Shashi A1 - Hoffmann, Per A1 - Hofmann, Andrea A1 - Jamain, Stephane A1 - Jiménez, Esther A1 - Kahn, Jean-Pierre A1 - Kassem, Layla A1 - Kelsoe, John R. A1 - Kittel-Schneider, Sarah A1 - Kliwicki, Sebastian A1 - Koller, Daniel L. A1 - König, Barbara A1 - Lackner, Nina A1 - Laje, Gonzalo A1 - Lang, Maren A1 - Lavebratt, Catharina A1 - Lawson, William B. A1 - Leboyer, Marion A1 - Leckband, Susan G. A1 - Liu, Chunyu A1 - Maaser, Anna A1 - Mahon, Pamela B. A1 - Maier, Wolfgang A1 - Maj, Mario A1 - Manchia, Mirko A1 - Martinsson, Lina A1 - McCarthy, Michael J. A1 - McElroy, Susan L. A1 - McInnis, Melvin G. A1 - McKinney, Rebecca A1 - Mitchell, Philip B. A1 - Mitjans, Marina A1 - Mondimore, Francis Mark A1 - Monteleone, Palmiero A1 - Mühleisen, Thomas W. A1 - Nievergelt, Caroline M. A1 - Nöthen, Markus Maria A1 - Novák, Tomas A1 - Nurnberger, John I. A1 - Nwulia, Evaristus A. A1 - Ösby, Urban A1 - Pfennig, Andrea A1 - Potash, James B. A1 - Propping, Peter A1 - Reif, Andreas A1 - Reininghaus, Eva A1 - Rice, John A1 - Rietschel, Marcella A1 - Rouleau, Guy A. A1 - Rybakowski, Janusz K. A1 - Schalling, Martin A1 - Scheftner, William A. A1 - Schofield, Peter R. A1 - Schork, Nicholas J. A1 - Schulze, Thomas Gerd A1 - Schumacher, Johannes A1 - Schweizer, Barbara W. A1 - Severino, Giovanni A1 - Shekhtman, Tatyana A1 - Shilling, Paul D. A1 - Simhandl, Christian A1 - Slaney, Claire M. A1 - Smith, Erin N. A1 - Squassina, Alessio A1 - Stamm, Thomas A1 - Stopkova, Pavla A1 - Streit, Fabian A1 - Strohmaier, Jana A1 - Szelinger, Szabolcs A1 - Tighe, Sarah K. A1 - Tortorella, Alfonso A1 - Turecki, Gustavo A1 - Vieta, Eduard A1 - Volkert, Julia A1 - Witt, Stephanie H. A1 - Wright, Adam A1 - Zandi, Peter P. A1 - Zhang, Peng A1 - Zollner, Sebastian A1 - McMahon, Francis J. T1 - Genome-wide association study of 40,000 individuals identifies two novel loci associated with bipolar disorder N2 - Bipolar disorder (BD) is a genetically complex mental illness characterized by severe oscillations of mood and behavior. Genome-wide association studies (GWAS) have identified several risk loci that together account for a small portion of the heritability. To identify additional risk loci, we performed a two-stage meta-analysis of >9 million genetic variants in 9,784 bipolar disorder patients and 30,471 controls, the largest GWAS of BD to date. In this study, to increase power we used ~2,000 lithium-treated cases with a long-term diagnosis of BD from the Consortium on Lithium Genetics, excess controls, and analytic methods optimized for markers on the Xchromosome. In addition to four known loci, results revealed genome-wide significant associations at two novel loci: an intergenic region on 9p21.3 (rs12553324, p = 5.87×10-9; odds ratio = 1.12) and markers within ERBB2 (rs2517959, p = 4.53×10-9; odds ratio = 1.13). No significant X-chromosome associations were detected and X-linked markers explained very little BD heritability. The results add to a growing list of common autosomal variants involved in BD and illustrate the power of comparing well-characterized cases to an excess of controls in GWAS. Y1 - 2016 UR - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/72382 UR - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-723824 N1 - Preprint, später in Human Molecular Genetics doi: 10.1093/hmg/ddw181 ER -